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Andrew D. Randall - One of the best experts on this subject based on the ideXlab platform.

  • The Neuroprotective Agent sipatrigine (BW619C89) potently inhibits the human tandem pore-domain K+ channels TREK-1 and TRAAK
    Brain research, 2001
    Co-Authors: Helen J. Meadows, Conrad Gerald Chapman, D.m. Duckworth, Rosemary E. Kelsell, Paul R. Murdock, S. Nasir, Gillian I. Rennie, Andrew D. Randall
    Abstract:

    We have cloned and functionally expressed the human orthologue of the mouse TRAAK gene. When cDNA for hTRAAK is expressed in either Xenopus oocytes or HEK293 cells it forms a K+-selective conductance and hyperpolarises the resting membrane potential. Quantitative mRNA expression analysis using Taqman revealed that hTRAAK mRNA is predominantly present in the central nervous system where it exhibits a regionally diverse pattern of expression. Like the related channel TREK-1, the activity of TRAAK was potentiated by arachidonic acid. The Neuroprotective Agent sipatrigine (10 μM) inhibited both hTREK-1 (73.3±4.4%) and hTRAAK (45.1±11.2%) in a reversible, voltage-independent manner. Inhibition of both channels was dose-dependent and for TREK-1 occurred with an IC50 of 4 μM. The related compound lamotrigine, which is a better anticonvulsant but weaker Neuroprotective Agent than sipatrigine, was a far less effective antagonist of both channels, producing

  • the Neuroprotective Agent sipatrigine bw619c89 potently inhibits the human tandem pore domain k channels trek 1 and traak
    Brain Research, 2001
    Co-Authors: Helen J. Meadows, Conrad Gerald Chapman, D.m. Duckworth, Rosemary E. Kelsell, Paul R. Murdock, S. Nasir, Gillian I. Rennie, Andrew D. Randall
    Abstract:

    We have cloned and functionally expressed the human orthologue of the mouse TRAAK gene. When cDNA for hTRAAK is expressed in either Xenopus oocytes or HEK293 cells it forms a K+-selective conductance and hyperpolarises the resting membrane potential. Quantitative mRNA expression analysis using Taqman revealed that hTRAAK mRNA is predominantly present in the central nervous system where it exhibits a regionally diverse pattern of expression. Like the related channel TREK-1, the activity of TRAAK was potentiated by arachidonic acid. The Neuroprotective Agent sipatrigine (10 μM) inhibited both hTREK-1 (73.3±4.4%) and hTRAAK (45.1±11.2%) in a reversible, voltage-independent manner. Inhibition of both channels was dose-dependent and for TREK-1 occurred with an IC50 of 4 μM. The related compound lamotrigine, which is a better anticonvulsant but weaker Neuroprotective Agent than sipatrigine, was a far less effective antagonist of both channels, producing <10% inhibition at a concentration of 10 μM.

Helen J. Meadows - One of the best experts on this subject based on the ideXlab platform.

  • The Neuroprotective Agent sipatrigine (BW619C89) potently inhibits the human tandem pore-domain K+ channels TREK-1 and TRAAK
    Brain research, 2001
    Co-Authors: Helen J. Meadows, Conrad Gerald Chapman, D.m. Duckworth, Rosemary E. Kelsell, Paul R. Murdock, S. Nasir, Gillian I. Rennie, Andrew D. Randall
    Abstract:

    We have cloned and functionally expressed the human orthologue of the mouse TRAAK gene. When cDNA for hTRAAK is expressed in either Xenopus oocytes or HEK293 cells it forms a K+-selective conductance and hyperpolarises the resting membrane potential. Quantitative mRNA expression analysis using Taqman revealed that hTRAAK mRNA is predominantly present in the central nervous system where it exhibits a regionally diverse pattern of expression. Like the related channel TREK-1, the activity of TRAAK was potentiated by arachidonic acid. The Neuroprotective Agent sipatrigine (10 μM) inhibited both hTREK-1 (73.3±4.4%) and hTRAAK (45.1±11.2%) in a reversible, voltage-independent manner. Inhibition of both channels was dose-dependent and for TREK-1 occurred with an IC50 of 4 μM. The related compound lamotrigine, which is a better anticonvulsant but weaker Neuroprotective Agent than sipatrigine, was a far less effective antagonist of both channels, producing

  • the Neuroprotective Agent sipatrigine bw619c89 potently inhibits the human tandem pore domain k channels trek 1 and traak
    Brain Research, 2001
    Co-Authors: Helen J. Meadows, Conrad Gerald Chapman, D.m. Duckworth, Rosemary E. Kelsell, Paul R. Murdock, S. Nasir, Gillian I. Rennie, Andrew D. Randall
    Abstract:

    We have cloned and functionally expressed the human orthologue of the mouse TRAAK gene. When cDNA for hTRAAK is expressed in either Xenopus oocytes or HEK293 cells it forms a K+-selective conductance and hyperpolarises the resting membrane potential. Quantitative mRNA expression analysis using Taqman revealed that hTRAAK mRNA is predominantly present in the central nervous system where it exhibits a regionally diverse pattern of expression. Like the related channel TREK-1, the activity of TRAAK was potentiated by arachidonic acid. The Neuroprotective Agent sipatrigine (10 μM) inhibited both hTREK-1 (73.3±4.4%) and hTRAAK (45.1±11.2%) in a reversible, voltage-independent manner. Inhibition of both channels was dose-dependent and for TREK-1 occurred with an IC50 of 4 μM. The related compound lamotrigine, which is a better anticonvulsant but weaker Neuroprotective Agent than sipatrigine, was a far less effective antagonist of both channels, producing <10% inhibition at a concentration of 10 μM.

Eduardo Moya - One of the best experts on this subject based on the ideXlab platform.

Ian S. Blagbrough - One of the best experts on this subject based on the ideXlab platform.

Ahmed E. Abdel Moneim - One of the best experts on this subject based on the ideXlab platform.

  • The Neuroprotective effects of purslane (Portulaca oleracea) on rotenone-induced biochemical changes and apoptosis in brain of rat.
    CNS & neurological disorders drug targets, 2013
    Co-Authors: Ahmed E. Abdel Moneim
    Abstract:

    Purslane (Portulaca oleraceae L.), a member of the Portulacaceae family, is widespread as a weed and has been ranked as the eighth most common plant in the world. In order to evaluate purslane herbal aqueous juice as a Neuroprotective Agent, the antioxidant activity of purslane juice was assessed in vitro and the Neuroprotective effects of purslane (1.5 mL/Kg bwt) on rotenone (12 mg/Kg bwt for 12 days) induced biochemical changes and apoptosis in striatum of rats were also examined. The repeated administration of rotenone produced dramatic increases in intercellular content of calcium, dopamine metabolites and apoptosis in the striatum. In addition, rotenone administration caused significant decrease in complex I activity. These biochemical changes and apoptosis inductions were effectively counteracted by administration of purslane. Overall, the present study demonstrated the Neuroprotective role of purslane in the striatum and proposes its prophylactic potential against developing brain damage and Parkinson's disease induction followed by rotenone administration, and that purslane may be considered as a potential Neuroprotective Agent against environmental factors affecting the function of the dopaminergic system.

  • the potential role of portulaca oleracea as a Neuroprotective Agent in rotenone induced neurotoxicity and apoptosis in the brain of rats
    Pesticide Biochemistry and Physiology, 2013
    Co-Authors: Ahmed E. Abdel Moneim, Mohamed A Dkhil, Saleh Alquraishy
    Abstract:

    Abstract Portulaca oleraceae (purslane), a member of the Portulacaceae family, is widespread as a weed and has been ranked the eighth most common plant in the world. In order to evaluate purslane herbal aqueous juice as a Neuroprotective Agent, we assessed the anti-apoptotic and antioxidant effects of purslane (1.5 ml/kg bwt) on rotenone (12 mg/kg bwt) induced brain injury in rats. Our results showed that purslane significantly decreased the number of apoptotic cells in the striatum. Immunohistochemical detection of nuclear factor kappa B (NF-κB) and B-cell lymphoma-2 (Bcl-2) showed that after purslane treatment there was an increase in cells stained positively for Bcl-2 and a decrease in the cells stained positively for NF-κB indicating the anti-apoptotic effect of purslane due its antioxidant activity. The elevation in reactive oxygen species, thiobarbituric acid reactive substances, nitrite/nitrate and lactate dehydrogenase were all reduced with purslane treatment. Furthermore, PCR results for iNOS and caspase-3 genes showed down-regulation in purslane treated groups. Overall, our study emphasizes the pro-survival role of purslane in the midbrain and striatum and proposes its prophylactic potential against developing brain damage and neurodegenerative diseases associated with oxidative stress.